Ataxia (and Dysmetria)
Alexander R. Toftness in Incredible Consequences of Brain Injury, 2023
These difficulties with planned movement, especially with the hands and eyes, can be described in terms of dysmetria. Dysmetria is a difficulty in moving a body part to the intended position. For example, dysmetria may include moving a muscle too far or not moving it enough. Trying to pick up a glass of water may result in knocking the glass over by moving the hand too far. If a person tries to move their eyes to look at something, they may not move their eyes far enough and therefore fail to look at the thing. Moving a muscle too far is called hypermetria, while not moving it far enough is called hypometria (Timmann & Diener, 2003). The person may need to readjust their hand or eye position multiple times. Dysmetric movements exist both in large movements, such as in the legs, and in small movements, such as in the fingers, and are more inaccurate when movement is attempted quickly (Hore et al., 1991).
Neurological Examination of Malingering
Alan R. Hirsch in Neurological Malingering, 2018
The finger-to-nose test is used to detect dysmetria. In this test patients are asked to touch their nose with the tip of their index finger, followed by reaching out to touch the examiner’s finger. When repeating this process the examiner will place his or her finger at different locations for the patient to touch. In true ataxia, patients will produce a side-to-side oscillating tremors which is not smooth and increases with amplitude distally, but eventually they will touch the examiner’s index finger. Malingerers dissimulate, as if unable to touch their finger to their own nose (Figure 3.12a). They may circle around the nose with wandering movements which would eventually lead them to touching the very tip of their nose (Figure 3.12b). Making exaggerated movements while being able to touch the tip of the nose is difficult compared to the normal performance of the finger-to-nose to test. Some patients may constantly tap one part of the face to demonstrate that they cannot touch their nose (Figure 3.12c). These positive findings can invoke suspicion for malingering (Campbell, DeJong, and Haerer, 2005).
Discussions (D)
Terence R. Anthoney in Neuroanatomy and the Neurologic Exam, 2017
Some other authors, however, define dysmetria so narrowly that it seems to include only hypermetria. For example, Gilroy and Meyer equate “dysmetria” with “past pointing” (1979, p. 54), as does Chusid—“Dysmetria (past-pointing phenomenon)” (p. 197). One recent medical dictionary also contains a similar definition of “dysmetria”: “A form of dysergia in which the subject is unable to arrest a muscular movement at the desired point” (Hensyl, 1982, p. 433).
Morphologic characterization of the anterior inferior cerebellar artery: a direct anatomic study
Published in Neurological Research, 2020
L.E. Ballesteros, P.L. Forero, H.Y. Estupiñan
The AICA occlusion results in a syndrome that mainly compromises the cerebral stem and the middle cerebellar peduncle, present in wide clinical presentations that may include: paralysis of the facial and vestibulocochlear nerves caused by the involvement of the nerves and their nuclei; vertigo, nausea, vomiting and nystagmus caused by injuries of the vestibular nuclei and their connections to the nuclei of the decimal cranial nerve, ipsilateral anaesthesia and thermal analgesia on the face and corneal hypoesthesia, caused by interruption of the trigeminal fascicle; Horner’s syndrome determined by the interruption of the descending pupil dilating nerve fibers located on the lateral portion of the pons and the medulla oblongata; hypoesthesia and thermal analgesia in the contralateral hemi body due to compromise of the lateral spinothalamic fascicle [19]; also, cerebellar ataxia and asynergy attributed to a lesion in the lower cerebellar peduncles [4,20–23]. Furthermore, dysarthria, ipsilateral dysmetria may also occur. Additionally, a loss of ipsilateral conjugate gaze as a consequence of flocculus involvement. Finally, it is worth mention that infarctions of the AICA territory are rare and often misdiagnosed [24].
Emergency surgery for brainstem cavernoma haemorrhage with severe neurological presentation. Is it indicated and worthwhile?
Published in British Journal of Neurosurgery, 2020
Cristiano M. Antunes, Renata S. F. Marques, Maria J. S. Machado, Leandro T. M. Marques, Miguel A. R. Filipe, João S. Fernandes, Carlos M. G. Alegria
This 31-year-old female’s symptoms started with right-side hypoesthesia, ataxia and diplopia. After one month of the onset of the symptoms, she was investigated with head CT and MRI, which revealed a pontomesencephalic cavernoma with evidence of recent haemorrhage (Figure 5(a)). She was initially treated ‘conservatively’ but, after four days, she suddenly developed a severe headache, nausea and vomiting, depression of conscious level to GCS 13 (O3V4M6) and MRI showed there was an increase in hematoma volume (Figure 5(b)). She was then emergently operated through IV ventricle floor with ultrasonography support after EVD placement at Frazier’s point. The hematoma and cavernoma were removed (Figure 5(c)). She was admitted to the Intensive Care Unit for a short period. She was discharged to rehabilitation with progressive improvement. She was operated on by the Ophthalmology to correct diplopia caused by III nerve paresis and VI nerve palsy. At the last follow-up, she was able to walk with support despite residual right-side ataxia and a grade 4 right-side hemiparesis. She had severe right-side dysmetria – mRankin 4.
Spinocerebellar ataxia type 7 with RP1L1-negative occult macular dystrophy as retinal manifestation
Published in Ophthalmic Genetics, 2019
Jun Young Park, Seo Young Wy, Kwangsic Joo, Se Joon Woo
A 52-year-old female patient with a medical history of hypertension visited the Neurology outpatient clinic presenting with gait disturbance and dysarthria that had begun 5 years earlier. The patient’s father had a history of cerebellar atrophy, and her younger brother had symptoms similar to her symptoms (Figure 1). She had mild dysmetria on the finger-to-nose and finger-to-finger test. Visually, she was noted to have hypermetric saccade and impaired smooth pursuit eye movements. A magnetic resonance image demonstrated mild cerebellar atrophy. Genomic DNA was isolated from peripheral blood leukocytes using a DNA isolation kit (Gentra PureGene; Gentra Systems Inc, Minneapolis, Minnesota). The CAG trinucleotide repeat region within ataxin-7 allele was amplified using the fluorescent-labeled fragment through polymerase chain reaction on a thermal cycler followed by capillary electrophoresis on the ABI PRISM 3100 Genetic Analyzer (Applied Biosystems, Foster City, California). The sizes of the repeats were determined by comparing fragments with the standard curve using GeneMapper version 4.1 software. DNA analysis revealed 39 CAG repeats on the ataxin-7 gene; hence, a diagnosis of SCA7 was made.
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